Nonsteroidal anti-inflammatory drugs (NSAIDs) block prostaglandin and prostacyclin biosynthesis via their inhibition of cyclooxygenase (COX) enzymes. By inhibiting COX-1, aspirin reduces thromboxane production, and this leads to its antiplatelet effect. By more effectively inhibiting COX-2, other NSAIDs have relatively greater anti-inflammatory, antipyretic, and analgesic effects. The adverse effect profile of nonselective NSAIDs includes bleeding, particularly gastrointestinal bleeding, which is thought to result from gastric irritation, antiplatelet effects, and the loss of prostaglandin-mediated mucosal repair.1 Selective inhibitors of COX-2 were developed with the hope they would have fewer gastrointestinal adverse effects and would be highly effective against chronic inflammatory states, such as arthritis.
Campbell CL, Moliterno DJ. Potential Hazards of Adding Nonsteroidal Anti-inflammatory Drugs to Antithrombotic Therapy After Myocardial Infarction: Time for More Than a Gut Check. JAMA. 2015;313(8):801–802. doi:10.1001/jama.2015.0567
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